Colonization with two different subtypes in DSS-induced colitis mice is associated with strikingly different microbiome and pathological features.

The gut microbiota plays a significant role in the pathogenesis of inflammatory bowel disease (IBD). However, the role of infection and -altered gut microbiota in the development of inflammatory diseases and their underlying mechanisms are not well understood. We investigated the effect of ST4 and ST7 infection on the intestinal microbiota, metabolism, and host immune responses, and then explored the role of -altered gut microbiome in the development of dextran sulfate sodium (DSS)-induced colitis in mice.

Experimental colonization with Blastocystis ST4 is associated with protective immune responses and modulation of gut microbiome in a DSS-induced colitis mouse model.

Background: Blastocystis is a common gut protistan parasite in humans and animals worldwide, but its interrelationship with the host gut microbiota and mucosal immune responses remains poorly understood. Different murine models of Blastocystis colonization were used to examine the effect of a common Blastocystis subtype (ST4) on host gut microbial community and adaptive immune system.

Results: Blastocystis ST4-colonized normal healthy mice and Rag1 mice asymptomatically and was able to alter the microbial community composition, mainly leading to increases in the proportion of Clostridia vadinBB60 group and Lachnospiraceae NK4A136 group, respectively.